Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Chemoreceptor Cells”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 181 records · Page 10Linked to original sources
PubMed1977

Caffeine restores feeding response to 2-deoxy-D-glucose in 6-hydroxydopamine-treated rats.

A large portion of the central catecholaminergic nerve terminals of the rat are destroyed by administering 6-hydroxydopamine (6-HDA) via the cerebrospinal fluid. Animals lesioned in this way often appear normal, yet show many subtle behavioural abnormalities. We have been examining one example of this phenomenon, the failure of 6-HDA-lesioned rats to increase food intake when given a systemic injection of 2-deoxy-D-glucose (2-DG) (refs 5, 6). This glucose analogue seems to elicit feeding in intact rats due to its inhibition of glycolysis in cerebral chemoreceptor cells. We have proposed that lesioned animals do not eat because of an insufficient central catecholaminergic response to the severe decrease in glucose utilisation induced by 2-DG (ref. 10). If so, then pretreatments which serve to augment this neurochemical response might be expected to reinstate behavioural function. Consistent with this hypothesis, very large increases in telencephalic tyrosine hydroxylase activity in 6-HDA-lesioned animals, which occur following chronic insulin treatment, are associated with the restoration of 2-DG-induced feeding. Many of the physiological effects of catecholamines in the sympathetic nervous system seem to be mediated by an increase in the cyclic AMP concentration of the target cells. Methylxanthenes, such as caffeine and theophylline, inhibit phosphodiesterase, prevent cyclic AMP degradation, and thereby potentiate the catecholamine-stimulated rise in cyclic nucleotide. They also enhance many of the behavioural and physiological effects of catecholamines, presumably by the same mechanism. We therefore sought to determine whether the acute administration of those sympathomimetic agents, in intact and 6-HDA-lesioned rats, also would potentiate 2-DG-induced feeding, a behaviour that seems to be mediated, in part, by central catecholaminergic neurons. We report that caffeine restores the 2-DG-induced feeding response.

Animals↗
PubMed2000

A metabotropic glutamate receptor variant functions as a taste receptor.

Sensory transduction for many taste stimuli such as sugars, some bitter compounds and amino acids is thought to be mediated via G protein-coupled receptors (GPCRs), although no such receptors that respond to taste stimuli are yet identified. Monosodium L-glutamate (L-MSG), a natural component of many foods, is an important gustatory stimulus believed to signal dietary protein. We describe a GPCR cloned from rat taste buds and functionally expressed in CHO cells. The receptor couples negatively to a cAMP cascade and shows an unusual concentration-response relationship. The similarity of its properties to MSG taste suggests that this receptor is a taste receptor for glutamate.

Amino Acid Sequence↗
PubMed1997

Arterial and venous paragangliomas: the value of a preoperative pacemaker and a multidisciplinary approach.

Non-chromaffin paragangliomas are very rare tumours. They arise from chemoreceptor cells at multiple sites throughout the body. They are usually very vascular and most arise in intimate contact with vital structures making their excision a surgical challenge. We describe in this paper four cases of paragangliomas in the carotid body and the jugular bulb. Their presentation was unusual. Two cases underwent excisional surgery and two had radiation treatment because they were not fit for surgery. We had to use a temporary pacemaker for preoperative preparation of the carotid body because of an associated hypersensitive carotid sinus syndrome. The clinical presentation and the surgical management will be described in this paper.

Adult↗
PubMed1994

In vitro activation of cyclo-oxygenase in the rabbit carotid body: effect of its blockade on [3H]catecholamine release.

The release of prostaglandin E2 (PGE2) from rabbit carotid bodies (CBs) incubated in basal conditions (PO2 approximately 132 mmHg; PCO2 approximately 33 mmHg; pH = 7.42) amounts to 94.4 +/- 10.1 pg (mg protein)-1 (10 min)-1 (mean +/- S.E.M.). Incubation of the CB in a hypoxic solution (PO2 approximately 46 mmHg) produced a significant 40% increase (P < 0.05) in the release of PGE2. Indomethacin (2 microM) prevented the hypoxia-induced release of PGE2. Sensory plus sympathetic denervation of the CB 4 days prior to the experiments did not modify either basal or low PO2-induced PGE2 release, indicating that intraglomic nerve endings are not significant sources for the PGE2 released. Incubation of the CB in an acidic-hypercapnic solution (PO2 approximately 132 mmHg; PCO2 approximately 132 mmHg; pH = 6.60) or in a high K(+)-containing solution (35 mM) was also effective in promoting an increase in the outflow of PGE2 from the organs. The release of [3H]catecholamines ([3H]CA) from the CB elicited by incubating the organs in low PO2 solutions (PO2 ranged between 66 and 13 mmHg) was potentiated by two inhibitors of cyclo-oxygenase, acetylsalicylic acid (ASA, 100 microM) and indomethacin (2 microM). The effect persisted after chronic denervation of the organ. The secretory response elicited by acidic stimuli was also augmented by cyclo-oxygenase inhibitors. Thus, [3H]CA release elicited by incubating the CBs in the acidic-hypercapnic solution increased by 300% in the presence of indomethacin (2 microM), and ASA (100 microM) more than doubled the release induced by dinitrophenol (100 microM), a protonophore that mimics an acidic stimulus. Indomethacin, but not ASA, moderately increased the high K(+)-evoked [3H]CA release. The effect of indomethacin on the release of [3H]CA elicited by acidic and hypoxic stimuli was reversed by PGE2 in a dose-dependent manner (0.3-300 nM). These results show that low PO2 and high PCO2-low pH, the natural stimuli to the CB, as well as high extracellular [K+], activate the cyclo-oxygenase pathway in the CB, promoting an increase in the outflow of PGE2. The data also show that the blockade of this pathway activates the stimulus-induced [3H]CA release from the CB, indicating that naturally released prostanoids exert an inhibitory control on chemoreceptor cells. The data lend support to the notion that the hyper-reactivity of the ventilatory response to hypoxia in subjects under anti-inflammatory drug treatment results from CB cycloxygenase inhibition.

Animals↗
PubMed1999

Potential identification of the O2-sensitive K+ current in a human neuroepithelial body-derived cell line.

Whole cell recording of H-146 cells revealed that the outward K+ current was completely inhibited by quinidine (IC50 approximately 17 microM). In contrast, maximal concentrations of 4-aminopyridine (4-AP; >/=10 mM) reversibly blocked only approximately 60% (IC50 approximately 1.52 mM). Ten millimolar 4-AP had no effect on the inhibition by hypoxia, which reduced current density from approximately 27 to approximately 13 pA/pF, whereas 1 mM quinidine abolished the hypoxic effect. In current clamp, 10 mM 4-AP depolarized the cell by approximately 18 mV and hypoxia caused further reversible depolarization of approximately 4 mV. One millimolar quinidine collapsed the membrane potential and abrogated any further hypoxic depolarization. RT-PCR revealed expression of the acid-sensitive, twin P domain K+ channel TASK but not of TWIK, TREK, or the known hypoxia-sensitive Kv2.1, which was confirmed by sequencing and further PCR with primers to the coding region of TASK. However, a reduction in extracellular pH had no effect on K+ current. Thus, although the current more closely resembles TWIK than TASK pharmacologically, structurally the reverse appears to be true. This suggests that a novel acid-insensitive channel related to TASK may be responsible for the hypoxia-sensitive K+ current of these cells.

Base Sequence↗
PubMed1998

Intracellular calcium changes and chemosensitivities of human epidermoid carcinoma cell lines after exposure to cisplatin.

In order to elucidate the mechanisms of cisplatin (cis-diamminedichloroplatinum; CDDP)-resistant tumor cells, we previously established a CDDP-resistant KB cell line (KBrc cells) from a parental KB cell line derived from epidermoid carcinoma (KB cells). The KBrc cells were resistant to 5 kinds of platinum (Pt) drugs. Intracellular Pt concentrations in KBrc cells were lower than in KB cells. Decrease of intracellular Pt concentrations was one of the CDDP-resistant mechanisms. When we measured changes of intracellular calcium ion concentration ([Ca2+]i) during exposure to high-dose CDDP, a sustained elevation of the [Ca2+]i level was observed in the KB cells. These results suggest that the mechanisms underlying CDDP resistance involve changes in calcium channels and an alteration of calcium homeostasis in the tumor cell line.

Antineoplastic Agents↗
PubMed2002

Poly(ADP-ribose) polymerase activity in the cat carotid body in hypoxia and hyperoxia.

Reactive oxygen species (ROS) induce DNA damage with the ensuing activation of the chromosomal repair enzyme poly(ADP-ribose) polymerase (PARP). ROS also interact with the function of carotid body chemoreceptor cells. The possibility arises that PARP is part of the carotid chemosensing process. This study seeks to determine the presence of PARP and its changes in response to contrasting chemical stimuli, hypoxia and hyperoxia, both capable of generating ROS, in cat carotid bodies. The organs were dissected from anesthetized cats exposed in vivo to acute normoxic (PaO2 approximately 90 mmHg), hypoxic (PaO2 approximately 25 mmHg), and hyperoxic (PaO2 > 400 mmHg) conditions. Carotid body homogenate was the source of PARP and [adenine 14C] NAD was the substrate in the assay. Specimens of the superior cervical ganglion and brainstem were used as reference tissues. We found that PARP activity amounted to 27 pmol/mg protein/min in the normoxic carotid body. The activity level more than doubled in both hypoxic and hyperoxic carotid bodies. Changes of PARP in the reference tissues were qualitatively similar. We conclude that PARP is present in the carotid body but the augmentation of the enzyme activity in both hypoxia and hyperoxia reflects DNA damage, induced likely by ROS and being universal for neural tissues, rather than a specific involvement of PARP in the chemosensing process.

Animals↗
PubMed2004

Malignant carotid body tumor: a case report.

Malignant carotid body tumors are rare neoplasms which originate from the chemoreceptor cells at the carotid bifurcation. A 61-year-old man presented with a neck mass which was diagnosed as a malignant carotid body tumor. Surgical resection of the mass with accompanying lymph nodes was performed. No evidence for local recurrence or distant metastasis were detected during the follow-up period.

Carotid Body Tumor↗
PubMed2006

Ultrastructural degradation of the carotid body in the aged rat: is there a role for atherosclerosis in the main carotid arteries?

In this study we examined the potential role of atherosclerosis in the main arteries supplying blood to the carotid body in the organ's morphological degradation with age. We addressed this issue by comparing the ultrastructural picture of carotid bodies and of fragments of the carotid artery bifurcation in two age-extreme groups of rats: young - 3 months old and senescent - 24 months old. Tissues were excised under surgical anesthesia, fixed in aldehydes, and processed for transmission electron microscopy. We found that the old carotid body parenchyma exhibited profound degenerative changes. Chemoreceptor cells were at various stages of atrophy, ranging from swollen mitochondria and fewer secretory vesicles to dark dehydrated cells. In contrast, the senescent carotid artery bifurcation was little different from that in young rats. Particularly, endothelial cells were in perfect condition. There were some changes in deeper arterial wall layers such as breaks in the continuity of elastic bands or a subtly different phenotype of smooth muscle cells. No foam cells or calcium build-ups were found in the arterial walls. Such changes correspond to the process of arterial wall stiffening in old age rather than to the outright atherosclerosis. Lack of atherosclerosis in the common carotid arteries, which could hamper blood flow, argues against its playing a role in the morphological age-changes in the carotid bodies.

Aging↗
PubMed1976

[Chemodectomas of the vagus nerve. Pathogenic hypothesis based on a review of 100 cases].

In connection with a personal case, 100 chemodectomas of the vagus described in the literature have been collected: revealing themselves in 75p. 100 of the cases in the form of cervical and pharyngeal tumours, 50p. 100 of the tumours of the vagal glomus involve some neurological manifestations mainly in the form of lesion of the lower cranial nerves. These appear to be either affected in isolation (41 p. 100) or in a dissociated manner (59 p. 100). Intra-cranial extension is rare (7 p. 100 of the cases) and delayed. Carotid angiography is characteristic. 76 p 100 are intra-vagal, 24 p. 100 are para-vagal and 60 p. 100 are located in the plexiform ganglion. Multifocal forms which account for 17 p. 100 of the cases are more usually, but not exclusively, familial. Surgical treatment is followed by sequelae or complications in more than half the cases. Close attention has been paid to pathogenetic theories: chemodectomas of the vagus may develop from type I chemoreceptor cells of the carotid glomera or from distinct cells with different properties (S.I.F. cells). They may equally well develop from nonchromaffin paraganglionic cells which have not migrated in the normal manner. The finding of such cells in the nerves of new-born babies and adults supports this theory, at least for some chemodectomas of the vagus.

Female↗
PubMed1982

Malignant nonfunctioning paraganglioma of the retroperitoneum producing renovascular hypertension.

Malignant nonchromaffin paraganglioma (chemodectoma) is an unusual tumor arising from chemoreceptor cells derived from the neural crest. Although these tumors generally occur in the head and neck, where the term "carotid body tumor" applies, more than 20 cases of retroperitoneal origin have been described. This case report presents the clinical, radiographic, and pathologic features of a chemodectoma arising in the retroperitoneal area that produced severe hypertension by unilateral real vascular compression. The patient underwent exploratory laparotomy, and a left nephrectomy was done. Follow-up examination 1 year after surgery disclosed no clinical evidence of disease, and he had normal blood pressures without medication.

Adult↗
PubMed1993

Multi-unit compartmentation of the carotid body chemoreceptor by perineurial cell sheaths: immunohistochemistry and freeze-fracture study.

The existence and extent of the perineurial cell envelope in the carotid body was clearly demonstrated by the immunoreactivity for nerve growth factor receptor (NGFR) and the freeze-fracture analysis. Consequently the chemoreceptor is regarded as multiple units, each of which consists of certain numbers of chief and sustentacular cells and nerves covered as a whole by a sheath of the perineurial cells.

Animals↗
PubMed1985

Oxygen chemoreception by carotid body cells in culture.

Chemoreceptors for oxygen reside within the carotid body, but it is not known which cells actually sense hypoxia and by what mechanisms they transduce this information into afferent signals in the carotid sinus nerve. We have developed systems for the growth of glomus cells of the carotid body in dissociated cell culture. Here we demonstrate that, as in vivo, these cells contain the putative neurotransmitters dopamine, serotonin, and norepinephrine. Oxygen tension regulates the rate of dopamine secretion from the glomus cells. Similar to chemically stimulated catecholamine secretion from other adrenergic cells this hypoxia-stimulated release requires extracellular calcium. These results are compatible with the suggestion that the glomus cells of the carotid body are chemoreceptor cells and that they signal hypoxia by regulated secretion of dopamine.

Adrenal Medulla↗
PubMed1993

Chronic hypoxia in vitro increases volume of dissociated carotid body chemoreceptors.

Exposure of humans or animals to chronic hypoxia results in enlargement of the carotid body, a respiratory organ that controls ventilation. The underlying mechanisms are unclear but involve hypertrophy of the chemoreceptor glomus cells. To test whether the latter response can occur independent of the circulation or neural inputs, we exposed cultures of dissociated rat carotid body to chronic hypoxia (2-3 weeks in 6% O2), and compared the 3-D cell volume of immunofluorescent, tyrosine hydroxylase positive (TH+) glomus cells, from data sets obtained by serial confocal microscopy. We found a dramatic increase in volume (3-4 x control) of hypoxia-treated TH + cells, suggesting that glomus cell hypertrophy during chronic hypoxia in vivo is likely due to a local effect of low PO2, rather than the production of ectopic growth factors.

Animals↗
PubMed1991

Contrasting effects of HEPES vs HCO3(-)-buffered media on whole-cell currents in cultured chemoreceptors of the rat carotid body.

In this study we compared the effects of physiological bicarbonate/CO2-buffered media (BBM) with the commonly used N-2-hydroxyethylpiperazine-N'-2-ethane-sulfonic acid (HEPES)-buffered media (HBM) on whole-cell currents in cultured rat arterial chemoreceptors (i.e. glomus cells) using the perforated-patch technique. Two separate effects were observed on switching from HBM to BBM. First, in the majority of cells tested (31 of 36) there was an increase in the leakage conductance (ca. 5 fold) and a concomitant increase in channel noise, which in preliminary studies appears to arise from the opening of large-conductance anion channels. Second, there was a reversible decrease in voltage-activated outward K+ current which we attribute to cytoplasmic acidification, catalysed by carbonic anhydrase in glomus cells.

Animals↗
PubMed1999

Acid-evoked quantal catecholamine secretion from rat phaeochromocytoma cells and its interaction with hypoxia-evoked secretion.

1. Amperometric recordings using polarized carbon fibre microelectrodes were used to detect exocytosis of catecholamines from rat phaeochromocytoma (PC12) cells in response to a reduction in pHo. 2. Exocytosis was detected at pHo levels of between 7.2 and 6.8. This was probably due to intracellular acidification, since acid-evoked secretion was enhanced by the Na+-H+ exchange blocker ethylisopropylamiloride (30 microM), and was mimicked by sodium propionate (10 mM), which causes selective intracellular acidosis. 3. Acid-evoked exocytosis was abolished by removal of Ca2+o or application of 200 microM Cd2+. It was unaffected by nifedipine, but significantly reduced by either omega-conotoxin GVIA (1 microM) or omega-agatoxin GIVA (200 nM). The two toxins applied together almost completely abolished (> 97 %) acid-evoked secretion. 4. Hypoxia-evoked catecholamine release was potentiated under acidic conditions and suppressed under alkaline conditions in a manner which indicated a greater than additive interaction of these two stimuli. 5. Our results indicate that, like carotid body arterial chemoreceptors, PC12 cells represent model chemoreceptor cells for both hypoxia and acidity and that the release of catecholamines in response to these physiological stimuli is dependent on Ca2+ influx through voltage-gated N- and P/Q-type Ca2+ channels.

Animals↗
PubMed2002

Conserved amplification of chemotactic responses through chemoreceptor interactions.

Many bacteria concentrate their chemoreceptors at the cell poles. Chemoreceptor location is important in Escherichia coli, since chemosensory responses are sensitive to receptor proximity. It is not known, however, whether chemotaxis in other bacteria is similarly regulated. To investigate the importance of receptor-receptor interactions in other bacterial species, we synthesized saccharide-bearing multivalent ligands that are designed to cluster relevant chemoreceptors. As has been shown with E. coli, we demonstrate that the behaviors of Bacillus subtilis, Spirochaete aurantia, and Vibrio furnissii are sensitive to the valence of the chemoattractant. Moreover, in B. subtilis, chemotactic responses to serine were increased by pretreatment with saccharide-bearing multivalent ligands. This result indicates that, as in E. coli, signaling information is transferred among chemoreceptors in B. subtilis. These results suggest that interreceptor communication may be a general mechanism for modulating chemotactic responses in bacteria.

Bacteria↗